2. Rheumatoid arthritis (RA) is a chronic
systemic inflammatory disease predominantly
affecting diarthrodial joints and frequently a
variety of other organs.
Peak incidence is between 4th and 6th decade.
Females are two to three times more affected
than males.
Genetic and autoimmune factors are mainly
responsible for the initiation of disease
process.
3. The pathologic hallmark of RA is synovial
membrane proliferation and outgrowth
associated with erosion of articular
cartilage and subchondral bone.
There is role of both cellular and
humoral immune mechanism in the
onset of inflammation.
4. Small joints of Hand-Pain/Stiffness > 1HR.
The pattern of joint involvement is typically
polyarticular and symmetrical and involves-
proximal interphalangeal (PIP)
metacarpophalangeal (MCP)
wrist, elbow, shoulder, knee, ankle,MTP joints
and cervical spine.
The distal interphalangeal (DIP) joints of the
fingers are usually spared.
5.
6. FEVER/MALAISE/HEADACHE
JOINT SWELLING/TENDERNESS.
With persistent inflammation, a variety of
characteristic joint changes develop like-
Z-deformity
Swan neck deformity
Boutonniere deformity.
7.
8. CLINICAL.
MRI IOC for early detection of
disease
ULTRASOUND
X-RAYS.
CT SCAN.
SYNOVIAL FLUID ASPIRATION
ANEMIA,RAISED ESR…
SEROLOGICAL TESTS.
9. Guidelines for classification
a. Four of seven criteria are required to classify
a patient as having rheumatoid arthritis (RA).
b. Patients with two or more clinical diagnoses
are not excluded.
10. Criteria
a. Morning stiffness: Stiffness in and around the
joints lasting 1 h before maximal improvement.
b. Arthritis of three or more joint areas: The 14
possible joint areas involved are right or left
proximal interphalangeal, metacarpophalangeal,
wrist, elbow, knee, ankle, and
metatarsophalangeal joints.
11. c. Arthritis of hand joints: Arthritis of wrist,
metacarpophalangeal joint, or proximal
interphalangeal joint.
d. Symmetric arthritis: Simultaneous
involvement of the same joint areas on both
sides of the body.
e. Rheumatoid nodules: Subcutaneous nodules
over bony prominences, extensor surfaces, or
juxtaarticular regions observed by a physician.
12. f. Serum rheumatoid factor: Demonstration of
abnormal amounts of serum rheumatoid factor.
g. Radiographic changes: Typical changes of
RA on posteroanterior hand and wrist
radiographs that must include erosions or
unequivocal bony decalcification localized in or
most marked adjacent to the involved joints.
13.
14.
15. Most common type of arthritis.
Leading cause of disability in elderly.
Much more common in women than men.
Definition: OA is joint failure,a disease in
which all parts of joint have undergone
pathologic change.initial step in the onset of
disease is failure of joint protective mechanism.
Joint vulnerability and joint loading are the two
major factors in development of disease.
16. Primary osteoarthritis is mostly related to aging. With aging, the
water content of the cartilage increases, and the protein makeup
of cartilage degenerates.
Secondary osteoarthritis is caused by another disease or
condition. Conditions that can lead to secondary osteoarthritis
include obesity, repeated trauma or surgery to the joint structures,
abnormal joints at birth (congenital abnormalities), gout, diabetes,
and other hormone disorders.
19. Cartilage is the primary target tissue for OA.
There is nonuniform loss of the cartilage.
Evidense of new bone formation is presence of
osteophytes.
There is as assymetric and nonuniform
involvement of the joints.
Capsule may become edematous and fibrotic.
Joint space narrowing is present as seen in all
types of arthritis.
20.
21.
22. Symptoms
Pain
o Joints may ache, or the pain may feel burning or sharp. For some people, it may get
better after a while.
o Pain while sleeping or constant pain may be a sign that arthritis is getting worse.
Stiffness
o When you have arthritis, getting up in the morning can be hard.
o Joints may feel stiff and creaky for a short time, until get moving.
o May also get stiff from sitting.
The muscles around the joint may get weaker
o This happens a lot with arthritis in the knee.
Cracking and creaking
o Joints may make crunching, creaking sounds.
Limited range-of-motion
23.
24. X-RAY-although used for evaluating OA ,are
insensitive for identifying early disease
process. They correlate poorly with patients
symptom.
Synovial fluid analysis-WBC’s count more than
1000/microlitre indicate inflammatory arthritis
and less likely OA.
ULTRASOUND.
MRI.
CT-scan.
BONE SCAN.
26. RHEUMATOID A.
Inflammatory.
Symmetric involvement
of small joints first.
Polyarticular.
Other visceral organs
also affected.
Erosion of adjuscent
bony surface.
Morning stiffnes>1hr.
OSTEOARTHRITIS
Degenerative.
Asymmetric
involvement of large
joint first.
Generally
monoarticular.
Not affected.
Sclerosis of adjuscent
bony surface with
osteophyte formation.
Morning stiffnes<1hr.
27.
28. A metabolic disease characterized by
recurrent attack of acute inflammatory
arthritis caused by elevated levels of uric
acid in the blood (hyperuricemia).
Most common rheumatic disease of
adulthood
The uric acid crystallizes and deposits in
joints, tendons, and surrounding tissues.
Hyperuricemia :
overproduction/underexcretion/both
Hyperuricemia ≠ Gout
29. 1. Acute gout
Acute, self limiting, monoarticular
Painful, red, hot, swollen
Usually resolves within 2 weeks if untreated
May occur even if serum urate is normal
LL > UL
Commonly affected joints
I. 1st metatarsophalangeal joint (podagra)
II. Forefoot/instep
III. Ankle joint
IV. Knee joint
V. Wrist joint
VI. Elbow joint
VII. Finger joints
Extra-articular : olecranon bursa, Achilles tendon
O/E : erythematous, warm, swelling over involved joint with
extreme tenderness +/- fever skin desquamation
Duration : 2 – 3 weeks, with gradual complete resolution of
inflammatory signs
30. 2. Intercritical gout
Asymptomatic period between attacks
3. Chronic gout
Polyarticular arthritis + tophi formation
Articular tophaceous gout may results in destructive
arthropathy and secondary OA
Tophaceous disease more like to occur in patients with:
Polyarticular presentation
Serum urate level >540 μmol/L (>9mg/dL)
Disease onset at younger age (≤40 years)
Sites of tophi
Digits of hands and feet (most common)
Pinna of ear (classic, less common)
Bursa around elbows and knees
Achilles tendon
31. Two of the following criteria are required
for clinical diagnosis :
1. Clear h/o at least 2 attacks of painful joint
swelling with complete resolution within 2
weeks
2. Clear history or observation of podagra
3. Presence of tophus
4. Rapid response to colchicine within 48 hours of
treatment initiation
Definitive diagnosis : presence of
monosodium urate crystals seen in synovial
fluid/tissues
32. Specific investigations for confirmation
Serum uric acid
Joint aspiration and crystal identification
Not widely available
To detect medical conditions a/w gout or hyperuricemia
FBC
Serum creatinine/urea
Serum blood glucose
Fasting lipid profile
UFEME
24h urinary urate excretion :
Useful if renal calculus proven to be urate stone
Indicated if on uricosuric agent
Assess risk of stone
Help to indicate whether overproduction or underexcretion of urate
Range : 2-4 mmol/24h or 0.34-0.67g/24h
To detect complications
Renal imaging
Skeletal x-rays
33. Skeletal x-rays
Acute gouty arthritis : normal; soft tissue
swelling
Chronic tophaceous gout : tophi, erosive bone
lesions (punched out lesions), joint space is
preserved until late stage, pathognomonic in foot
and big toe
34. Contributing factors eg. thiazide/loop
diuretics; low dose aspirin may be discontinued
or substituted, if appropriate
Pharmacotherapy of asymptomatic
hyperuricemia is NOT necessary, except :-
Persistent severe hyperuricemia
- > 770μmol/L (13mg/dL) in male
- > 600μmol/L (10mg/dL) in female
Persistent elevated urinary excretion of urate
- > 0.65mmol/L/day (11mg/day), a/w 50% increased
risk of urate calculi
Tumor lysis syndrome
- chemotherapy/radiotherapy extensive tumor
cytolysis => require pre-hydration and allopurinol to
prevent acute urate nephropathy
35. Initiation within 24 hours of onset
If on Allopurinol, continue without interruption
NSAIDs
eg. Diclofenac, indomethacin, mefenemic acid etc
Caution in h/o PUD, HPT, renal impairment, IHD, liver impairment
COX-2 inhibitors (celecoxib, etoricoxib, parecoxib) = alternative for
above risk factors
Studies have shown that etoxicoxib (Arcoxia) has equal efficacy to
indomethacin
Colchicine
Inhibiting mitosis and neutrophils motility and activity, leading to a
net anti-inflammatory effect.
Alternative drug if CI to NSAIDs, but is poorly tolerated by elderly
Therapeutic index is narrow
Slower onset of action
Evidence base for prophylaxis is stronger than for NSAIDs (NHS Fife, Gout
Management Guidelines, 2010)
SE (eg. N&V, abd. pain, profuse diarrhea) limit its usefulness
Dosage : 0.5mg – 0.6mg BD-QID
36. Last resort for gouty arthritis
Removal of tophi
Joint fusion
Joint replacement
Ulceration of tophi : debridement, dressing
with sodium bicarbonate solution
Indications for chronic tophaceous gout :
Advanced tophi deposition resulting in major joint
destruction
Loss of involved joint movements a/w severe pain
Tophi collection causing pressure symptoms, eg
carpal tunnel syndrome of wrist
Tophaceous ulcer
Cosmetic eg ear lobe tophi